Unit 6 and Unit 7 Part 1 Flashcards
influenza
acute viral infc in URT
when does influenza increase
seasonal infc
which types of influenza have inc prevelance
types A, B,C
incubation period for influenza
1-4 days
what strain of influenza usually causes epidemics
A
who has inc risk for influenza
HCP
peds pts
geri pts
why do HCP have inc risk for influenza
personally compromised rt repeat exposure
why do peds pts have inc risk for influ
defenses arent fully established yet
why do geri pts have inc risk for influ
dec defenses rt to age
patho influenza
viral injury to epithelial cells in URT, inflm/tissue damage
why may abx be perscribed in influ
prophylaxis ONLY, to dec risk of 2ndary infc rt compromised IR in pts w inc susceptibility
2 complications assoc with influ
2ndary bact infc
bronchitis/pnumonia
what are complications of influ rt to
movement of virus to LRT lt bronchial/alveolar damage
mnfts
cough
fever
malaise
characteristics of cough in influ
beneficial unless the URT is irritated, then it inc irritation/infc -> damage
course of influenza
self limiting
tx of influenza
prevent spread vaccine for prophylaxis symptomatic mgmt limit infc to urt antivirals??
egs of antivirals
amantadine
rienza
amantadine
1st gen antiviral that inhibits RNA coating of virus
what strains is amantadine most effective against
A and B
rienza
2nd gen antiviral that inhibits replication of virus, prevents virus rls from host
pnuemonia
inflm of bronchioles and alveoli
what forms does pnuemonia come in
infectous
non infectous
what is pnuemonia classifed by
agent
location
et of pnuemonia
usually dt bact, or virus, fuingu
aspiration
inhalation of fumes
how does inflm occur in pnuemonia
agent enters RT and proceeds into lungs
why is it abn for an infectous agent to proceed into the lungs
pulmonary defense is impaired and cant filter out pathogens
what happens when there is inflm in the lungs in pnuemonia
pulm edema -> impaired gas exch -> Co2 build up -> systemic hypoxia
typical pnuemonai
bacterial pnuemonia that occurs where there is empty spaces
atypical pnuemonia
dt any other agent, virus? things proliferating using cells around tissues
lobar pnuemonia
lung inflm specific to an entire lobe
broncho pnuemonia
inflm throughout alveoli in entire lung
area of consolodation
area with solidification of 3 components
what 3 components make up areas of consolodation when solidified
exudate
inflm debris
inflm cells
how are areas of consolidation seen
on cxr
mnfts of pnuemonia
fever/chills dyspnea rt dec gas exchnage sputum headace chest pain
what mnft makes pnuemonia different the flu
chest pain
sputum
combination of mucous and exudate
dx for pnuemonia
hx, px
cxr
sputum c and s
why are sputum c and s’s done in pnuemonia
to determine if abx are needed
tx of pnuemonia
abx with typical pnuemonia
symptomatic mgmt
COPD
persistant inflm causing aw, vasculature and parenchyma inflm
what episodic problem is prominent in copd
acute, recurrent, chronic obstr of aw
what disorder are included in copd
chronic bronchitis
emphysema
what may copd coexist with
aasthma
et/risks for copd
smoking (80-90%)
recurrent resp infc (not chronic)
aging
genetic def of alpha one antitrypsin
why does aging inc risk for copd
lt dec lung compliance rt age of aw and l/o elasticity
what does smoking do to mucous prod? what does it lead to
inc mucous in RT, lumenal obstr
how does smoking compromise the mucociliary blanket
destroys cilia that lines the RT
how does inc mucous in RT affect cilia
overwhelms them by mucous logging them
what does smoking do to the airway
inflames it
what effect does smoking produce? (mnft)
coughing
what does coughing do to the airway of the copd pt
inc damage to inflamed area
what structures of the RT does smoking destroy
aw
alveoli wall
3 mechanisms of airflow in chronic bronchitis (CB)
hypertrophy of bronchial wall
inflm and mucous sec
damage to elastic tissue
hypertrophy of bronchial wall in CB
lt dec lumen size dt inc inflm
inflm and mucous sec in CB
lt up to 50 percent lumen obstr. dt inflm causing inc exudate and smoking lt inc mucous
damage to elastic tissue in CB
lt dec compliace, airway is no longer held open
what is CB dt
smoking, reccurent infc
where do changes in CB appear first
large aw
characteristics of affected large aw in CB
hypertrophy of submucousal glands rt inc gland workload
why do submucosal glands of inc workload in CB
dt inc sec of mucous dt smoking
where do changes appear second in CB
smaller airway
what changes occur in the smaller aw in CB
inc in goblet cells
what does inc/excess mucous in CB lt
impaired mucociliary defense
what happens when mucociliary defenses are compromised in CB
infc and bronchial wall inflm
why does aw collapse occur in the patho of CB
lumen obstr rt inflm leads to collapse caused by trapping of air in terminal aw. air slowly diffuses out into circulation lt collapse
what happens do alveolar ventilation in CB, why
decreases, dt air trapped in parts of lung
what happens when there is a V:P imbal
hypoxemia
hypoxemia
dec O2 in ABG
V in V:P
air moving in and out lungs
P in V:P
gaseous exchange
normal V:P
0.8
normal V
4L air in and out/min
normal P
5.5L blood thru PC /min
what is important to remember about VP ratio
it could be the same number even if V and P are smaller, abn numbers
what variable changes in CB
why
V
dt abn obstr. even though aw may collapse, its still a ventilation problem, not perfusion
dx CB
chronic cough (cant use coughing alone)
chronic cough
presence of cough for 3 consec mo for 2 years
main mfnt of CB
impaired resp fx
how is impaired resp evidenced by
hypoxemia
hypercapnia
resp fx
composed of gas exch and ventilation
other mnfts of CB (7)
activity intol inc mucous prod sputum dyspnea wheezing w/o auscultation wet crackles inc expiratory length
what is dyspnea in CB dt
lumen obstr
what is wheezing dt in CB
thinning aw
why are wet crackles heard in auscultation in CB
air moving over and thru mucous
why is expiration length inc in CB
rt dec elastic recoil of lungs -> trouble compressing TC to exhale quickly
complication of CB
secondary bact infc rt mucous accum
emphysema
destr of alveolar tissue and capilarry beds
what are of lung has inc incidence for emphysema
terminal airway
what does emphysema lt
l/o compliance
compliance
ease of lung filling/emptying with inc difficulty breathing
what happens to distal airspace in alveoli in emphysema
increases dt loss of wall integerity
what causes enlarged distal airspaces in emphysema
alveolar merging
why is alveolar merging not beneficial
inc alveolar size -> inc SA -> dec surface for gas exchange
et emphysema
smoking (classic)
genetic def of alpha1 antitrypsin (A1A)
fx of A1A
protease, ez inhibitor, allows break down of old protein in an organized and controlled fashion
what is A1A responsible for
regulating protein breakdown in lungs
what does smoking do to A1A in classic emphysema
inhibits it
what happens when a1a is inhibited
inflm and protein break down in lungs
what does cigarette smoke attract to the lungs
inflm cells
what do inflm cells bring to lungs
inc proteases
what do proteases do to the lungs
alveolar damage
how is smoking with classic emphysema a triple wammy in terms of patho and lung damage
inhibits inhibitor
increases inflm cells
inflm cells bring inc protease
why is ventilation impaired in emphysema
permanent distended air spaces
what VP variable does emphysema change
Both
why is WoB inc in emphysema
air is trapped in spaces between alveoli
what does trapped air result in
increased amount of dead space
dead space
areas not involved in gas exchange
why is ventilatory effort in emphysema increased
rt dec/compromised lung capacity
what 3 things mean increased work of breathing
nasal flaring
pursed lip breathing
accessory m use
why does the P variable change in emphysema
capillary walls are destroyed by proteases -> impaired perfusion
another name for air pocket inbetween alveoli
bleb
bullae
when a bleb inc in size and is visible bc it presses on plueral memb
what does smoking lt (fig flowcart)
attraction of inflm cells
dec a1a activity
what is released when inflm cells are attracted (fig flowchart)
elastase
what inhibits the action of elastase (fig flowchart)
a1a
what causes destruction of elastic fibers in lungs (fig flowchart)
dec a1a dt smoking
inherited a1a def
inhibited elastase action
what does destruction of elastic fibers lead to in lungs (fig flowchart)
emphysema
2 types of emphysema
centraacinar
panacinar
centriacinar emphysema
destruction is confied to terminal and respiratory bronchi.
alveoli condition in centriacinar emphysema
currently have little damange
which type of emphysema is most common
centraacinar
panacinar
damage to aw and peripheral alveoli
inc severity
mfnts of emphysema
dyspnea
inc ventilatory effor
barrel chest
what makes something a barrel chest
when chests transverse diameter and anterioposterior diameter are equal (2:2)
what is a normal chest diamter ration
2:1 transverse to anterioposterior
dx for COPD
hx, px
labs
cxr
pulm fx tests
what do pulm fx tests measure
lung vol
tx for COPD
limit progression
lifestyle mod
vaccine
drugs
what lifestyle mods have to be made to tx copd
NO smoking
avoid aw irritants
why do we encourage COPD pts to get vaccianted
for prophylaxis rt dec IR and inc susceptibility
what vaccinations should copd pts receive
flu q1 year
pnuemonial q5year
first line drugs for COPD
short acting b receptor agonist
anticholinergics
what happens if first line drugs arent working for COPD
add inhaled steroids
what do we do if a short acting b receptor agoinst isnt working COPD
long acting b receptor agonist
thcophyline (COPD)
bronchodilator with some anti inflm properties
how do beta receptors work
cause bronchodilation in bronchiols (smaller aw)
how do anticholinergics work
cause bronchodilation in larger aw (bronchi)
